ABS-201 Androgenetic Alopecia KOL Seminar

Good morning everyone. Thank you for joining our deep dive today into ABS 2011. At ABSI, our mission is to use

2011. At ABSI, our mission is to use generative AI to create better biologics for patients who don't have good enough options today. We talk a lot about our

options today. We talk a lot about our platform, our lab in the loop, and our ability to create better biologics faster. But today isn't just about the

faster. But today isn't just about the platform in the abstract. Today is about the results. ABS 2011, which we believe

the results. ABS 2011, which we believe could be a paradigm changing therapeutic for androgenic alopecia.

Now, historically, the bioarm industry has dismissed hair loss as just cosmetic. But when you speak to

cosmetic. But when you speak to patients, you realize that characterization is deeply flawed. For tens of millions of people, both men and women, this is

not about vanity. It's about identity.

It's about mental health and a profound loss of confidence that impacts their daily lives. Despite this massive unmet

daily lives. Despite this massive unmet medical need, the standard of care has remained stagnant for decades. We're

relying on old mechanisms that often come with difficult tradeoffs. This is

why we're so excited about ABS 2011. By

leveraging our AI drug creation platform, we have unlocked the prolactin receptor pathway in a way that we believe offers a differentiated

best-in-class profile. We have an

best-in-class profile. We have an incredible agenda for you today. It

follows the journey from the patient to the antibbody to the market. First,

you'll hear from Dr. Rossi who will lay the groundwork in the patient reality and the psychosocial impact of hair loss. Then we'll move into the science.

loss. Then we'll move into the science.

Andreas will discuss his long history with the mechanism and why he's so excited to finally see this brought forward into clinical trials. Professor

Ralph Paws, a world expert on hair biology, will walk you through the mechanism of action and the compelling Xvivo data we've generated. Next, Dennis

and Dr. Sinclair will detail our clinical trial design. Dr. Sinclair's

experience with the prolactin receptor mechanism is unparalleled.

He will explain why he believes this trial is set up for success. Finally,

Dr. Goldberg, Mike Jafar, and Zach Jonison will define the target product profile necessary to change the treatment landscape.

They will walk us through the significant commercial opportunity that lies ahead. We believe ABS 2011 is more

lies ahead. We believe ABS 2011 is more than just an asset. It is proof of what happens when you combine deep biological insight with the speed and precision of

generative AI. But before we get into

generative AI. But before we get into the data, I want to ensure we start where every drug development journey should start, with the patient. We'll

play a short video that captures the reality of living with AA. After that,

I'll hand it over to Dr. Rossi. Thank

you for being here. Let's watch.

>> My name is Kelly Caesars. I have three kids, a husband. I'm from Wisconsin, middle school and high school teacher. I

hope they would describe me as kind, um, funny occasionally. Um, a lover. I Yeah,

funny occasionally. Um, a lover. I Yeah,

I hold my family really close to the heart. It would have been my junior year

heart. It would have been my junior year cuz I was living in an apartment. Um,

and I just noticed in the shower that like a ton of hair was falling out. I

already had my like thyroid checked and I had um, you know, the vitamin defic all that stuff checked that they say you should get checked and it all came out normal. So, kind of my last stop was a

normal. So, kind of my last stop was a dermatologist and um she was the one who said I had the female pattern baldness and they said there were medications

available but they didn't recommend them if I was going to have kids or if I wanted to have kids and I I did want kids so that wasn't an option. And so I basically kind of left like I literally

think I called my now husband and I was like we need to lock down a date cuz I'm balding and I need to make sure you're locked in for life because I'm losing my hair. So let's set a date. I have my

hair. So let's set a date. I have my topper in right now. And this is kind of how I do it every day. I'll take it off so you can kind of see

um where my hair loss is thinning.

So, my part is kind of starting to widen and you can see like at the top it's like when you can start seeing the scalp that drives me nuts.

And then the really bad spots are the crown of my head, which is where the hair thinning started from the get-go.

And it's just slowly getting worse.

It's a struggle that I have. I don't

always love the way that I look. Um,

but again, that doesn't make all of me like that's just one piece of me. And I think that's been the biggest

me. And I think that's been the biggest thing. And that is a

thing. And that is a daily struggle that I have to tell myself.

It's exhausting.

Yeah, it sucks.

And I don't I don't want my daughters and my son to see me as someone that doesn't love themselves cuz

I don't want I want them to love themselves and never think they're less than.

Sorry.

So, I just will keep faking it till I really believe it.

I'm not wrong for feeling this way.

There should be a solution and people should be paying attention. I wish there was actually something that would like not just thicken the hair I already have

but regrow the hair that I have lost.

Like that is what I want. If science

could eliminate hair loss, that would be the dream.

Um, as a kid, I remember very vividly being five and six years old, scoring a goal, feeling the adoration from the parents on the sideline or my teammates.

And that translated to being a professional, scoring goals, and feeling the love and adoration from the crowd.

And that was almost an addictive cycle that I wanted to feel more of that. And

it propelled me to score more. I'm

Landon Donovan. I played soccer for 14 years for the Los Angeles Galaxy and the US men's national team. I was fortunate to play in three World Cups. I scored

five goals, which is the most all time for the US men's national team. I won

six MLS Cup championships. I proudly

lifted 11 trophies in my career and over 150 games played for the US men's national team. I don't know the exact

national team. I don't know the exact age, probably 22 or 23. I wasn't losing hair, but my hairline was receding. And

and I would start looking and look back on earlier pictures and I was like, "Oh, it was here and now it's here." And in warm-ups or during the game, I would hear people start making comments about

my hair and they would say, "Hey, looks like your hair's falling out, Lanner.

You're getting bald, Landon." As the internet became the internet, there were so many comments about receding hairline and look how bald Landon is. And then it would happen also in the stadium. So it

was just this constant dribble about it all the time. And over

time that starts to impact you knowing millions of people or tens of millions or hundreds of millions of people around the world are watching.

You feel helpless like there's nothing you can do about it. And so when you're on TV a lot it's right in front of people. They're not distracted by the

people. They're not distracted by the game and what's going on. They're just

looking at you in your hair. So it's

been exacerbated since I stopped playing. And sadly, unfortunately, so is

playing. And sadly, unfortunately, so is the receding. It's gotten worse and

the receding. It's gotten worse and worse. So, I went in at 25.

worse. So, I went in at 25.

25 years old, pretty young. The only

option that was viable was to get a hair transplant. I've taken oral medication,

transplant. I've taken oral medication, topical medication. I've tried it all.

topical medication. I've tried it all.

Um, now I have a hair system. Um, I've

I've tried everything and I've been desperate, I think like many many many millions of Americans, for something that will solve this problem once and for all.

>> The perfect situation is I have my real hair in my real head. I

mean that I would feel free. I I can feel it in my body that would feel so free and I desperately want that back. I

think in the past people view this as a vanity thing. For me, it's not vanity.

vanity thing. For me, it's not vanity.

It's a disease. I know how this impacts human beings. It's impacting me and I'm

human beings. It's impacting me and I'm really grateful that ABSI is putting the resources and the funding into this.

Hi, I'm Dr. Rossi. I'm a boardcertified dermatologist and dermatologic surgeon.

I work at Memorial Sloan Kettering in New York City and there's not a day that goes by that I don't talk about hair loss with my patients. Hair loss for many patients is not just a cosmetic

issue. It's actually a medical problem

issue. It's actually a medical problem that affects them psychosocially, emotionally, and then their daily activities of living. We view hair as

something cultural, something religious, something that people identify with. uh

growing up with hairdressing parents and being in a hair salon my whole life, I really know that firsthand how how meticulous people are with their hair.

And so hair loss for me is not just something cosmetic. It's a disease that

something cosmetic. It's a disease that dermatologists want to tackle. They want

to treat and they want to improve their patients quality of life. It's akin to obesity. For many for many years, people

obesity. For many for many years, people didn't think obesity was a disease. They

thought it was more a cosmetic uh you know basically cosmetic issue but it's not. We know it's a disease. We know it

not. We know it's a disease. We know it represents something that's going on inside the body as well. And I view hair loss is that I try to get to a root cause analysis of why this patient's

losing their hair and how we can better treat them holistically. There's

different causes of hair loss. There's

different types of hair loss. But we do know above all that it really affects patients psychosocially. And not only is

patients psychosocially. And not only is it something that's going on physically, but emotionally it can really take a toll on patients and and even young patients and female patients. And we've

seen an uptick of female patients coming in for this. And this is driven by awareness. Back in the day, we didn't

awareness. Back in the day, we didn't have so much awareness of female female pattern hair loss. And now that more women are talking about it or describing it, it's really helped to bring this to

the forefront, especially for women. And

hair loss does affect everyone. We know

all ages, males, females, as you heard from Landon and Kelly, two different time points in their life, both affected by androgenetic alopecia. What's really

amazing is that I'm seeing patients that are highly motivated to tackle their hair loss. And this includes young men

hair loss. And this includes young men who sort of know that they have it coming down the genetic pipeline. They

see their parents with hair loss and they know they really need to address this early. as well as now females,

this early. as well as now females, which is amazing because they're talking more about hair loss even though there's a lack of FDA approved medications for it. They're talking more about it in the

it. They're talking more about it in the chat rooms and they're bringing it up in their in their consultation. They really

want to address their hair thinning and their hair loss, especially around the, you know, the 30s and 40s. It's really

critical for them. And this is something that we want to give options to patients, right? We don't want to just

patients, right? We don't want to just say, "Hey, there's this only medication that you can take." But if we had more medications that we could actually use in these populations that were safe,

efficacious, but also durable because we know we will have to be treating them for quite some time. And I'm really excited about the future of hair loss and for myself to treat hair loss.

That's because ABS 2011 represents a completely novel mechanism of action that we can use to help actually tackle hair loss and androgenetic alopecia. It

comes at hair loss in a completely new perspective than anything we've had before. And to hear more about the

before. And to hear more about the science of ABS 2011, the prolactin story, the mechanism of blocking the prolactin receptor, we're going to hear from Andreas Bush, who's going to go

over all that amazing research.

>> Hi, I'm Andreas Bush. I'm the chief innovation officer at APSAI.

Previously, I've been for many years in the industry being responsible for research and development at Bayer and at Shire.

Um in these times we have brought numerous projects towards clinical development and approval. I think um I would probably

approval. I think um I would probably account for more than 10 compounds being approved in my past. Um and I have to

say very few projects present themselves with uh such an excitement and uh potential as uh the

prolactin receptor antibbody which we're going to talk today about in our workshop.

It was at bear where we started work on prolactin. Prolleactin as the name says

prolactin. Prolleactin as the name says was obviously uh first discovered for

its role in lactation. Prolactation.

Um but uh what was also very obvious is that prolactin plays multiple roles in very different diverse

pathophysiological um events in human biology. We

identified a role in endometriosis but it was already at that time known that also prolactin could play a role in

hair growth. So we found that prolactin

hair growth. So we found that prolactin was responsible in a dual manner in endometriosis. On the one hand um it was

endometriosis. On the one hand um it was clearly uh playing a role in noception in the way women u perceive pain in

endometrials. On the other hand, it was

endometrials. On the other hand, it was um at least also in part responsible for the proliferation of endometrial cells which is of course the cause of the

lesions and the lesion size. As a

consequence, our thought was that uh inhibition of prolactin in endometriosis would have a dual mechanism too, which is of course reduce the lesion, would

therefore be disease modifying and of course also reduces the pain, which is the number one problem women really

perceive in endometriosis.

We obviously then developed an antibbody against prollein to study this antibbody

in the disease models and um not to our surprise it really nicely affected the proliferation of endometriosis in animal

models. Much to our surprise, there was

models. Much to our surprise, there was a more striking and obvious result which we got which is the shaved animals which

we had to shave for surgery for endometriosis models had a very rapid and significant hair growth. The hair

really grew like hell in those mice treated with the antibbody, thereby validating and confirming the previously

mentioned observation that prolactin could play a role in hair growth.

After the very compelling results in mice, we wanted to take that result one step further. We became aware of a

step further. We became aware of a naturally occurring androgenic alopeescia model in stumptail macak. And

again, believe me or not, what is a bigger dream of a pharmacologist than a naturally occurring disease model in a non-human primate?

Um, so we went into that primate. I

commissioned a study. Um and the result was just striking both in male as well as in female non-human primates. Uh we

saw a sustained hair growth and even further we saw repigmentation of the hair which at that point in those

non-human primates had already turned gray. The experimental design of this uh

gray. The experimental design of this uh macak study was um very um well thought

through. We treated the animals for 6

through. We treated the animals for 6 months. We dosed in a way that we

months. We dosed in a way that we assumed that we can see 90% occupancy of the prolactin receptors and we followed

up after 6 months of dosing these animals for several years. What we saw was um as already mentioned before

significant hair growth in some regions we saw doubling the hair um but we didn't just see significant hair growth but we saw repigmentation of

the already gray hair of those macak um not only that we saw that after 6 months we saw this in the follow-up period of up to four years in a

sustained manner.

So that certainly gave us very significant confidence that hair loss is indeed

dramatically affected by prolactin and the inhibition of prolactin in this androgenic alopecia setting can cause

hair regrowth together with the compelling efficacy results in non-human primates.

We of course were interested in the safety profile of the prolactin receptor antibbody. Uh we did the relevant preend

antibbody. Uh we did the relevant preend safety studies without any significant findings which we were of course very pleased about. But probably even more

pleased about. But probably even more important, we meanwhile got aware of genetic studies in females in which a

complete knockout of the prolactin receptor was shown. And this complete knockout of the prolactin receptor antibbody

caused nothing in that woman except a problem with lactation. but no other health concerns which of course gives us

again additional confidence in the safety of prolactin receptor antagonism.

So despite though those compelling results on the efficacy and safety of prolactin receptor antibbody in hair

loss we at the time did not further uh follow up on development in halos for numerous reasons. A hair

loss was not in our strategic focus.

Um a indication like hair loss was considered not appropriately treated with biologics or injections that was

considered uh an application which should be reserved to other indications.

So similar to other indications uh a learning curve had to be taken. uh

this learning curve which we saw in the industry was taken by GMP1 agonists I believe where in obesity

um the application of injectable peptides resulted in a complete new market situation in a situation where

patients understood the value of peptide injections. They were very much willing

injections. They were very much willing to pay out of their pocket for this indication.

And therefore we see that of course a safe and efficacious biologic in an indication such as hair loss is

something very viable and something very marketable. Beside being uh convinced

marketable. Beside being uh convinced about the mechanism being a tangible one for

hair loss, we also saw the shortcomings of this original antibbody. We saw that um the half-life was uh not the

half-life we wanted to see. The

solubility was not the solubility we wanted to see for an overall commercially attractive antibbody in hair loss. And when I arrived at Absi,

hair loss. And when I arrived at Absi, Sean and I very quickly discussed whether this would be an attractive

mechanism to a show that our platform, our AI platform works for generating a optimized antibbody where we can

simultaneously optimize several parameters of an antibbody and make this prolactin receptor antibbody a

commercially viable uh Um we started this task a little more than 2 years ago and we came up with an antibbody which

now does provide a halflife which we believe will enable us to apply the antibbody maybe every two to 3 months

only. We do think that we have an

only. We do think that we have an antibbody with a formulation which can be applied subcutaneously also very important for that indication.

Um, taking all of that together, we do believe that we now have generated with our platform a commercially highly

attractive antibbody.

I was for a very long time a believer in AI and the potential of AI in the entire value chain of R&D processes. Having

said that, it is extremely gratifying now to see that we are bringing a AI optimized antibbody into the clinic that

we will see that indeed the power of AI does translate to a clear benefit of the patient.

I talked about the multiple roles of prolactin in human biology both uh in pathophysiological settings

as well as in physiological settings. Of

course, one of the pioneers in the role of prolactin in hair growth is professor

Ps. Not only is Professor Poss an expert

Ps. Not only is Professor Poss an expert in hair follical biology, he will now work together with us to further

characterize the effectiveness and mechanism of ABS 2011 on hair follicle biology. With this, it's my privilege

biology. With this, it's my privilege and honor to hand over to Professor P.

Over to you.

>> My name is Ralph P. I'm a research professor of dermatology at the University of Miami Miller School of Medicine and I've worked for a long time

on hair research. In addition, we um have investigated neuro hormones of human

skin and in both areas uh we have done some pioneering studies and this is where the hair follicle enters the

picture. this tiny but miraculous mini

picture. this tiny but miraculous mini organ that makes hair shafts for example on your scalp. Uh this organ is so

special because it not only is highly responsive uh to numerous hormones which control its growth and hair shaft production and hair pigmentation but it

even makes these hormones themselves.

And uh the discovery that we made about um 20 years ago is that one of these hormones that is

hardly ever talked about in hair research is prollectin. Prolin is most famous for being the key hormone that controls milk production. That's where

the name comes from, prollectin. Um but

we now know that this hormone does multiple other things. uh it is controlling growth, it has immunore regulatory functions and uh about 20

years ago we we found that um not only do human scalp hair follicles um respond to stimulation with this hormone, in

fact they were inhibited when we micro dissected and organ cultured them by prolactin. But they even made prollectin

prolactin. But they even made prollectin themselves and this is where uh ABS 2011 comes in.

the prollectin receptor blocking antibbody developed by EPSI.

The company had read this uh old study and thought, well, could we perhaps promote human hair growth by blocking uh

the receptor um for this neuro hormone in order to keep the hair follicle longer in its growth phase and antigen

and uh thereby reduce the daily hair shaft shedding and get longerlasting uh effects than you would get with normal

drugs with a short halfife. life and uh we um uh used a system that we have been using for many years to study the effects of all sorts of hormones and

neuro hormones on human scalp hair follicles. What you can do is you can

follicles. What you can do is you can micro dissect these little organs um and uh then you throw them into an culture medium and crazily enough they still

grow as if they were on the living human scalp. And then in this essay as shown

scalp. And then in this essay as shown here on this slide uh you ask the question is my test substance in this case for example prollectin or the

prollectin receptor antibbody is that pushing the growing follicle the antigen follicle and you start with 100% antigen follicles in your culture is that

pushing the engine follicle faster into the regression phase kaggen or is it retaining it longer in antigen and if it retains it longer in antigen that means

you will have less hair loss. Um so what we are really looking for in this essay is on the right hand part of the slide

the transition of anogen follicles into ktoagen in this hair cycle. But in this case we studied it not in isolated micro

dissected hair follicles but we took the entire human scalp skin and specifically we used so-called temporaral scalp skin.

uh that is the scalp skin where androgenetic alopecia uh first becomes manifest uh in males.

And why did we take the entire scalp skin and and not micro dissected hair focus as we had done 20 years before? Um

we did that because we know that many cells in the skin have uh receptors for prolactin and can respond to it. And uh

we wanted to see how this antibbody um uh is impacting on hair follicles that are living in the real tissue

environment that they see in the living human body.

And uh what you do then is you take photos. You see this on the right hand

photos. You see this on the right hand side uh of scalp skin biopsies that uh you get from volunteers and you see what

is changing in the hair shaft production over six days.

Uh and then you take sections of these tissue fragments and you look at them under the microscope and you assess most and foremost what is happening with the

hair cycle. is are these hair follicles

hair cycle. is are these hair follicles staying longer in energy or do they go faster into catagen? That's the key question you have and then you can look at all sorts of additional markers that

get you a better idea of what exactly is happening. The first thing you need of

happening. The first thing you need of course to check in this system is does this antibbody even do uh what uh is

claimed um that it does. And uh

if you want to show that your antibbody in this case is blocking signaling through the prollein receptor, you have to show um that phosphorolated stud 5,

one of the signals that transmit a signal after stimulation of the receptor by prolactin is upregulated. And you see this in the green bar on the right hand

side. Uh that that's exactly what

side. Uh that that's exactly what happens. So if you stimulate scalp skin

happens. So if you stimulate scalp skin uh with prollectin then you get an upregulation of this signal and if you do this in the presence of the blocking

antibbody this is abrogated that uh was good news. So we know this antibbody is really active. It does what it's supposed to do at the level of the

prolactin receptor. And this perhaps is

prolactin receptor. And this perhaps is uh um the most uh important slide that we initially um the most important result

that we initially got. So we looked was there any effect on hair shaft production and uh as expected from our older studies in micro dissected hair

follicles. If we stimulated entire scalp

follicles. If we stimulated entire scalp skin, male scalp skin with prollectin, hair shaft production over six days was

reduced and um the uh follicles the number of follicles that stayed longer in uh anogen in the growth phase. You

see this by uh photo documenting that the hair shaft gets longer.

um was actually increased not only when you um co-cultivated prollectin with the prollectin receptor

antibbody but even by the prollectin receptor antibbody itself. That's the

bar on the um your second bar from the left in the center.

So that this antibbody alone has already hair growth promoting uh activities suggests that it is actually inhibiting prolactin that is locally made in the

hair follicle just at we as we had uh published many years ago and uh I was particularly interested to see this result and quite quite gratified because when we had first published this there

was lots of disbelief in the field that this actually is real but this is all macroscopic data that we see. So what

you can almost see with a naked eye. But

um the real litmus test is to use hisystological microscopic uh markers to prove that these follicles are really

longer in antigen and uh can that the antibbody against the prolactin receptor can antagonize the push towards kaggen that prolactin gives the product. That's

exactly what you see on this slide. So

again the antibbody alone the second bar from the left keeps hair focus long in its growth stage uh if you only give prollectin

they move into kadagen and if you give prollectin and the antibbody you um again have an antigen prolonging effect and then you can look at this more

fine-tuned and you can see what is the effect on cell proliferation and cell death aptosis in the actual hair shaft factory uh which is the so-called enigen

hair bulb the energen hair matrix and uh no surprise what you um see here is some is a phenomenon that perfectly um

supports what we had seen in terms of the hair cycle changes proliferation in the hair matrix is stimulated by this uh antibbody against the productin receptor

and cell death epitosis is reduced. And

note uh on the graph on the right hand side the blue bar the um impressive cell death protection effect of just the

prolactin antibbody prolin receptor antibbody itself. when we initially

antibbody itself. when we initially started um with his work and we discussed how to set up these experiments, I reminded um our

colleagues that um five years after our initial uh paper, we had found in female scalp hair follicles and if you blocked

the prolactin receptor um with a drug uh that may not have been as selective as this new prolactin receptor antibbody, the stem cells did not like it and went

into epitosis.

Therefore, we were nervous to see what would happen here in male scalp hair follicles in the stem cell compartment, the so-called bulge. And lo and behold,

the stem cells loved it. Uh the the epitosis actually went down when they were stimulated with this prollein receptor blocking antibbody. uh and um

in the presence of prollectin the stem cells even proliferated uh divided more uh than in the vehicle

control group. That was excellent news

control group. That was excellent news and is particularly interesting in a context of androgenetic alopecia because androgenetic alopecia

has uh two driving factors. One probably

critical driving factor is that the follicle gets smaller and smaller due to um missing inductive signals from the so-called dermma pillar at the at the

base of the um hair follicle. But the

other contributing factor uh is that the capacity of hair follicles to generate daughter cells from these stem cells uh is diminished.

So we looked at that too and interestingly um if you just give prollein that's the green bar on the left hand side of the slide

the number and expression of these cells that are daughter cells that are directly produced from these stem cells

gets reduced and uh if you give the prollectin receptor blocking antibbody this can be completely completely reversed. That is fascinating from an

reversed. That is fascinating from an androetic alopecia perspective because so far we have no drugs that can really

do that. Um so it appears that just

do that. Um so it appears that just blocking signaling through this one neuro hormone receptor

can um restore the capacity of hair focal stem cells to make daughter cells and thus keep the organ in its uh

desired large size. But that's not all.

Um when I first saw these slides I said what god what is this antibbody not doing? Um so it's actually improving the

doing? Um so it's actually improving the production of the key growth uh stimulating growth factors that the hair

follicle makes itself.

Um if you dump prolactin uh on your male scalp skin um the green bars uh then the production of uh key growth a key growth

factor called insulin like growth factor one IGF-1 goes down and even that of another important growth factor FGF 7

fibroid growth factor 7 goes down and uh that can be completely counteracted by adding the prollein receptor receptor antibbody. But even better,

antibbody. But even better, insulin growth factor one, the one growth factor that in human hair follicles keeps the follicle longest in

its growth phase, is stimulated just by the antibbody alone.

That means that just blocking the prollectin receptor um with this antibbody increases the capacity of the

hair follicle to produce growth factors itself with which it maintains and promotes its own growth. Yeah. And

finally we had shown before that uh you see this here again on the left hand side of the slide that um hair shaft production is stimulated by adding this

antibbody.

And if you see this microscopically, you would expect that also the production of hair shaft keratins um proteins that make the hair shaft is

upregulated and that's what you see in the graph on the center and in the imunofllororesence microscopy images on the right that that's exactly what happens.

So the antibbody has the capacity uh to um prolong the growth phase of the hair cycle and thereby reduce the daily hair

shaft shedding that dermatologists call tiggenlovium.

Um but it moreover uh also promotes hair focus stem cells themselves and specifically their capacity to produce

new daughter cells and to maintain this This would antagonize the andrrenic alopecia uh associated hair follicle

miniaturization process. And if as if

miniaturization process. And if as if this were not enough uh the antibbody also stimulates the follicle to make

more potent growth factors itself and to increase hair shaft production. Um very

very impressive. I did not expect that when we started this in in in um in in reality. I was fairly skeptical uh that

reality. I was fairly skeptical uh that any of this would happen but it did and um we repeated this in three donors and that's about uh the time point when you

feel confident um about your own data.

So in summary uh we're looking here at a antibbody that uh really blocks signaling through the prollectin receptor directly in human

scalp hair follicles in intact human scalp. So in the target organ that we

scalp. So in the target organ that we want to treat clinically and it does this on multiple levels. It on the one hand keeps the follicle longer uh in

antigen. uh on the other hand uh it

antigen. uh on the other hand uh it stimulates the production of growth factors that the follicle needs to remain an antigen and finally uh it even

stimulates stem cells uh and their capacity to generate new daughter cells and um also promotes hair shaft

production. That a single

production. That a single neuro hormone receptor antibbody could do all of this is highly unusual. I did

not expect it and I'm quite impressed by this. Until now, we discussed our data

this. Until now, we discussed our data from organ cultured male scalp skin. But

now it's time to talk about clinical trial data where we go from Xvivo to invivo. And this will be introduced by

invivo. And this will be introduced by Dennis followed by Professor Rod Sinclair from Melbourne.

>> Hi, my name is Dennis Akat. I'm VP

research at Absi and program lead for ABS 2011. uh within my role as VP in

ABS 2011. uh within my role as VP in research at ABSAI, I'm ensuring that the uh antibodies which the talented AI and web lab scientists create have a

seamless transition into the clinical development. Prior to joining ABSAI uh

development. Prior to joining ABSAI uh which was an amazing opportunity in my career I worked for a decade in big farmer across multiple indications

spanning from heart, lung, kidney and endometriosis in women's health. Um my

background is a trained biochemist with a PhD in neuroscience and also a training as laboratory geneticist. Um as

you have heard from Andreas um the prolactin receptor ABS 21 is one of this rare occasions as a geneticist where you really have these cases where human

mutation uh guide you with regard to the safety profile but also uh with the efficacy when we're looking into the mode of action and I'm very excited to

announce that we have uh dose our first participant in our headline trial the phase one to A study aims not only to

look into safety and tolerability as the main readout, but also we anticipate to have our interim efficacy readout in the second half of 2026. At Absite, we

always go big. This is why we have designed the ABS 2011 headline trial in a way where we not only combine safety and tolerability but also efficacy in a really fast way. So how do we do that?

So basically what we have thought about is how can we combine the pre-clinical readouts which we have from the monkey study and the Xvivo study in a really nice clinical trial design and I walk

you through that how we have outlined it. The headline trial is a

it. The headline trial is a double-blinded placebo control trial which aims to enroll up to 227 participants with and without androgenic

alopecia across single ascending dose and multiple ascending dose cohorts.

Within the SAD portion of our clinical trial where we are looking into up to four single ascending doses uh in healthy volunteers uh we will mostly assess um safety and tolerability but

also immunogenicity and what is most important pharmaccoinetic profile. So

how long is the halflife of the antibbody. We will then transition in

antibbody. We will then transition in the multiple ascending dose portion of the trial which has been designed in a way to be statistically powered to show hair growth efficacy throughout this uh

treatment duration. What do I mean with

treatment duration. What do I mean with that? Um when we're speaking about

that? Um when we're speaking about treatment is aeration. What you have heard earlier from Andreas is that within this naturally occurring androgenetic alopecia stumptail cake

model those monkeys were were treated for up to 6 months and we are aiming to do so for the healthy volunteers. So

this means that the healthy participants are dosed uh over 26 weeks and we will do a hair regrowth assessment at baseline at 13 week and then at 26 week

and then look at the hair regrowth progression over time. Based on the engineered long halflife of our antibbody we will follow up the participants for nearly a year and within this follow-up period we will

further interrogate uh the durability effect of the hair regrowth. The hair

regrowth assessment uh is measured by taking uh global images from the healthy volunteers but also what professor Paul taught you macroscopic images of the

scalp area where target area hair count, target area hair width and target area hair darkening is measured in order to get from this quantifiable variables

regulatory approved measures um for efficacy assessment. Aside of this

efficacy assessment. Aside of this quantifiable measurements, we will also have patient reported outcome measures which are very important because it's

one thing if you have really a numeric improvement, but it's really most important that the participant himself feels or sees that there's improvement on the hair regrowth in order to have

afterwards a quality of life improvement.

Of course, the next question is when are we going to have our insurance readout?

As mentioned earlier, we're treating our participants with androgenetic alopecia over a period of six months, mimicking not only what we have seen in the stumptail make study, but also

reflecting standard practice in hair regrowth trials. Within this six-month

regrowth trials. Within this six-month period, we will have a baseline assessment and then an assessment at 13we and then 26 week. Now, when are we expecting the first readout across all

three multiple ascending dose trials?

that will be as early as Q3, Q4 and 2026 and the 26 readout as early as beginning of 2027.

These readouts are important and will guide us in our registration or trials moving forward down the line. The

described phase one toa headline trial will take place in Australia within the multi-sight setup and we're super excited that one of the PIs will be

professor Rodney Sinclair who is a worldrenowned expert in androgenetic alopecia and will talk to you more about ABS 21 and the headline trial.

>> Hi, my name is Rod Sinclair. I'm the

professor of dermatology at the University of Melbourne and I've held that post for close to 20 years now and over the years hair loss has been my

passion. I wrote my my doctorate thesis

passion. I wrote my my doctorate thesis on androgenetic alopecia in women. I've

written multiple textbooks on hair loss.

I've written the the chapters on hair loss in Rook's textbook of dermatology and Bologna's dermatology textbook which are the the key textbooks that are used by dermatologists around the world. in

their training and so they've learned a lot about hair loss through those chapters. I've now published over a

chapters. I've now published over a thousand peer-review articles and average over the last 10 years at about one a week and we've done a lot of work in androgenetic alopecia. So I was

involved in the publication of the first genes for male patent baldness which was the androgen receptor and we did that through um gene association studies. We

also identified genetic linkage in female patent hair loss with the aromatase gene and the estrogen receptor gene. We have been involved in

gene. We have been involved in understanding the patterning of hair loss through epigenetic silencing of the androen receptor on the occipital scalp.

And we've also developed the main clinical grading scales used for female patent hair loss known aonomously as the Sinclair scale. So my clinic here in

Sinclair scale. So my clinic here in Melbourne is one of the largest dermatology centers in the Southern Hemisphere. We have over 20 specialist

Hemisphere. We have over 20 specialist dermatologists. We see over 70,000

dermatologists. We see over 70,000 patients per year, but we also integrate clinical research into our clinical practice. So we have one entire floor of

practice. So we have one entire floor of our building devoted to clinical trials.

We've done over the past 15 years over 300 industry sponsored clinical trials for pretty much all the major pharmaceutical players. And that goes

pharmaceutical players. And that goes from phase one through to phase 4. And

in androgenetic alopecia alone, we've probably done at least six uh phase three clinical trials developing products for for androgenetic alopecia.

So I've been interested in prolactin for over 25 years because one of my other roles has been as president of the Australasian hair and wool research society which is a a group that brings

together um scientists who do basic fundamental research on all mammals because of course the defining feature of mammals is hair and bring them together with the clinicians the dermatologists who are treating hair

loss and that's the the sister society of the American hair research society which you might be might be familiar with but the work that I was introduced to through my role in the Australian

hair research society centered around the way in which prolactin regulates the hair cycle in the psum. So the possum of course has seasonal molting. They have a winter coat and the summer coat and that

transition from the winter coat to the summer coat is regulated by prolactin.

And what you've probably just recently seen in the the fundamental research data prevent presented by professor pals is that prolleactin is a hormone that

has many more functions than simply inducing lactation. So certainly it's

inducing lactation. So certainly it's named because of its effect on uh women in the end of pregnancy in terms of activating their breasts to start to to

stimulate lactation. So it's a prolactin

stimulate lactation. So it's a prolactin prolactation hormone. But just because

prolactation hormone. But just because it's named for one thing doesn't mean it doesn't do many other things. And the

demonstration that prolactin is manufactured in the hair follicles. The

demonstration that prolactin has receptors in the hair follicles is testimony to the fact that this hormone is involved in regulation of the hair cycle doing things that people who were

thinking of it as a as purely a lactation hormone hadn't previously turned their mind to. And it turns out that it's actually a really important hormone in the regulation of hair

growth.

I think a lot of people have oversimplified the causation of male pattern baldness.

Many people have simplified the causation to be activation of testosterone into dihydrotestosterone.

dihydrotestosterone binding to androen receptors in the hair bulb that leads to miniaturaturization of the hair follicle and hey presto you go bald. What we've

been able to show is that the mechanism is actually much more complex. Before

you start to miniaturaturize the hair follicle you shorten the duration of the hair follicle growth cycle and that is something that involves the cyclical

regeneration of the hair follicles. So

what most people are aware of is that if you pluck a hair, new hair grows out of the same follicle. What many people haven't realized is that if you don't pluck a hair, a new hair grows out of that same follicle and just pushes the

old one out. And of course, the best example of that is that if you suddenly decided to start shaving your armpits, you'd see that the hairs are growing every day. But if you don't shave your

every day. But if you don't shave your armpits, they only grow so long and then the next year started to grow and it just pushes the old one out, which is a which is of course a good thing.

Otherwise, we'd have hairs poking out our sleeve. So that regulation of the

our sleeve. So that regulation of the hair cycle is the first thing to change in the onset of male pattern baldness

and that precedes the DHT mediated miniaturization of the hair follicle in the hair bulb and that shortening of the antigen duration is triggered by events happening at the top of the hair

follicle near where the erectyli or the or the goosebump muscle inserts into the hair follicle. And the other thing that

hair follicle. And the other thing that we've shown even more recently is that before you get miniaturaturization, you get disruption of the attachment of the

muscle to the hair follicle. So in fact that miniaturaturization of the hair bulb through DHT is actually a secondary and a late event in androgenetic

alopecia. It's probably permissive and

alopecia. It's probably permissive and it probably affects the patterning of the baldness, but it's not it's overstating it to say that that DHT binding to the androin receptor is the cause.

And so we want to see the upstream events that cause the baldness. We're

interested in the hair cycle changes.

And that's where the hormones that regulate the hair cycle such as prolactin suddenly start to come into play. And uh and that's where the the

play. And uh and that's where the the focus where the where the smart money is starting to starting to look. Now

what has started in Melbourne this week and will continue over the next 12 months is the headline trial which is the ABSI phase 1 phase 2a clinical trial

testing their their novel monoconal antibbody in healthy volunteers uh with and without androgenetic alopecia. So

the initial study is being conducted in a residential phase one clinical trial center which is about 2 kilometers down the road to the south and what we'll be involved in where I'm going to be the

principal investigator is the the phase 2a study investigating people with androgenetic alopecia and this is a

highly regulated highly controlled clinical trial. All the end points have

clinical trial. All the end points have been clearly established and the end points center around high quality photography. This is something that

photography. This is something that we've done before. It's something we've got great experience in and I think I can honestly say we produce, you know, the the highest quality clinical photog

clinical photographs available for for clinical research. The um the

clinical research. The um the recruitment is always a challenge in any clinical trial, but this is something that we've done before and in fact we've just closed recruitment on a trial with

140 participants for sublingual minoxidil in an androgenetic alopecia clinical trial and so we're very confident that we can uh recruit the lion share of participants for the for

the next for the next study. But of

course there are multiple sites in a competitive recruitment process and the aim for everybody involved is to complete the recruitment as uh as rigorously and as fast as possible with

of course no compromise on the quality of the the participants.

So the question on everybody's lips is what gives me as a dermatologist confidence that this trial can produce a

meaningful benefit for our patients.

Well, the first step is I think we're we're moving upstream in the mechanism of baldness. We're moving away from

of baldness. We're moving away from being fixated on the hair bulb and the miniaturaturization of the follicle to some of the earlier events through the regulation of the hair cycle. We know

from the animal models in first of all the possum that prolactin is involved in the regulation of the hair cycle. We've

seen experimental studies in the macak monkey when the macak monkey is probably the only animal model that reliably predicts treatment effects in

androgenetic alopecia. And I think

androgenetic alopecia. And I think there's some tantalizing interest from the macak monkey where there was a suggestion that even after the trial finished and the the dosing had stopped

that there was some ongoing benefit. Now

whether that happens in humans or not, we'll have to just wait and see. But I

think there's a lot of excitement in the patient world around this mechanism of approach to the treatment of androgenetic alopecia. And there's a lot

androgenetic alopecia. And there's a lot of excitement in the in the medical world to see how we can impact androgenetic alopecia looking at a variety of different targets beyond the

the historical target of the the five alpha reductase the DHT where the finasteride and related molecules were were focused on.

I was the the principal investigator in the in the phase 1B open label study for for hope with their molecule HMI115.

And this was an intravenous study. And

for hope, my impression was that this study was a bit of an afterthought and that their main focus was around endometriosis. And they were interested

endometriosis. And they were interested in uh in androgenetic alopecia as perhaps a a secondary a secondary market. And based on their phase one

market. And based on their phase one dosing, the doses that were selected for the androgenetic alopecia trial were probably a little bit too low. And the

reason I say that is that the receptor occupancy with the biologic therapy in the in the animal studies with the macac monkey and of course as I've said before

the macac monkey is the most reliable animal model for investigating androgenetic alopecia but the receptor occupancy in the macac monkey studies

was north of 90% whereas the receptor occupancy that was achieved in the HMI 115 hope medicine study was probably somewhere between about 60 and 80% but

probably south of 70%.

In contrast, ABSI have done some significant modifications directed by AI and they've led to better tissue distribution, better pharmaccoinetics

and specifically a longer halflife which is going to be attractive to the patients interested in pursuing this treatment. And we anticipate it's going

treatment. And we anticipate it's going to achieve greater than 90% receptor occupancy in the humans because of the dose they've selected. And as a consequence of that dose that achieves

higher receptor occupancy in the humans, we anticipate we're going to get more hair growth than hope achieved.

And so I will finish off here and I'm going to pass you over to Professor David Goldberg who's going to describe to you

the significant unmet need for a hair loss treatment that really shifts the dial amongst our patients. This is

something that everybody's been waiting for and uh and David Goldberg's the man to to tell you about it.

>> I'm Dr. David Goldberg. Uh I am the director of clinical research and cosmetic dermatology for the Schwiger dermatology group. Uh we are somewhat

dermatology group. Uh we are somewhat less than 200 offices from coast to coast uh Midwest eastern seabboard Florida. Uh I also run two uh fellowship

Florida. Uh I also run two uh fellowship programs in cosmetic dermatology through the American Society for Dermatologic Surgery. I practice cosmetic

Surgery. I practice cosmetic dermatology. Uh we've done a lot of

dermatology. Uh we've done a lot of research in the area of hair going all the way back to the 1980s and 90s with topical minoxidil. We've done some of

topical minoxidil. We've done some of the studies on plate rich plasma for hair. We've done some of the studies on

hair. We've done some of the studies on low-level light. Uh we're currently

low-level light. Uh we're currently involved in a trial for oral minoxidil through the FDA. Uh I run meetings uh just ran a meeting this past weekend uh called New Frontiers in Cosmetic

Medicine where we talked about the the current prolactin studies. Uh and we do a lot of research as well.

So the current standard of care for angenic alipcia frankly is is not very high. Uh as I mentioned uh we I was

high. Uh as I mentioned uh we I was involved in the topical minoxidil studies uh that's known as ro gain. Now

everybody comes in on that. That's not a prescription. Uh you know the numbers of

prescription. Uh you know the numbers of people seeking treatment for hair thinning are staggering. Uh if you look at men you know it's by the time they're 35 people are complaining. Women by the time they're 40. Women actually by the

time they're uh 65 80% of them complain of hair loss. And yet what do we do for them? Uh we have them on topical

them? Uh we have them on topical minoxidil. Uh you know that doesn't do a

minoxidil. Uh you know that doesn't do a lot. We start talking about platelet

lot. We start talking about platelet rich plasma and low-level light. In

order to do that they have to have their arms uh drawn blood. Uh that's painful.

It can lead to black and blue. We then

take that blood. We spin it down in a centriuge and then we reinject it into their scalps. That's a painful

their scalps. That's a painful procedure. They have to come into the

procedure. They have to come into the office. It's done once a month. And

office. It's done once a month. And

although we do a series of usually four or five treatments, it really is in perpetuity. So, they're constantly

perpetuity. So, they're constantly coming in on some of the men uh and some of the women. We give them uh what's called oral minoxidil. Now, it's not even FDA approved for hair loss. Uh it's

FDA approved for blood pressure. Uh the

dosages are really made for blood pressure. They're not made for hair

pressure. They're not made for hair thinning. Some people have problems with

thinning. Some people have problems with dizziness, dropping of blood pressure.

Some of the men we give oral finasteride uh that blocks testosterone the hormone that leads to hair thinning both in men and women and the problem with that in men is some of them get erectile

dysfunction. There's so much talk now on

dysfunction. There's so much talk now on social media about suicidal uh thought patterns in men who are taking that drug. You get a sense that the treatment

drug. You get a sense that the treatment approach right now is just not optimal.

And we currently don't have an ideal treatment for hair thinning. I mean

that's just pretty obvious. You know, if you look at surveys out there, less than 10% of people are happy with the current treatments we have. And so, what we want in a new hair treatment uh for hair

thinning and hair loss uh is something that is convenient. Uh doesn't have to be done that often, and it's got to be durable. Uh durable means, you know,

durable. Uh durable means, you know, they don't have to necessarily have an injection every week. They don't have to come into the office every month.

something that ideally they could do at home. You know, maybe they'll start

home. You know, maybe they'll start every week, but ultimately maybe every two months, every three months, something along that line. Uh, and we now are on the cusp of a drug that potentially can do that. And, you know,

this is such an exciting arena right now uh that I'm going to be discussing this uh at the end of January and meeting called MCCAST Paris. It's the largest cosmetic dermatology plastic surgery

meeting in the world. Uh there are some 20,000 people there. they all want to learn about this uh this new product, this new approach uh you know this prolactin receptor inhibition. It's a

very exciting area. So ABS 2011 clearly is a gamecher. One, it's a totally new mechanism. The fact that these hair

mechanism. The fact that these hair follicles have these receptors and then ABS 2011 now can block those receptors and convert resting non-growing

non-pigmented hairs into thick terminal growing darkened hairs is revolutionary.

So as I mentioned before um you know we we currently are involved uh in FDA studies uh for longer lasting minoxidal products allowing uh the higher dosage

to be given hopefully safer than is what currently available on the market but in the end you know that doesn't work the way ABS 2011 works. The way minoxidil works is it dilates blood vessels in the

area of the hair. It gives them more nutrition but it's not a direct impact on the hair. That's number one. Number

two, uh that's going to require compliance. People have to take pills

compliance. People have to take pills twice a day. What's exciting about ABS 2011 is how often people are going to need the drug. You know, we're looking initially at maybe two to three

injections over the first 6 months. But

think about it this way. Growing hairs,

they're called antigen hairs. They last

for a couple of years. And so if we get those injections, you know, two to three over 6 months, and then we're back in that growing hair stage, people are not going to need to do injection do injections very often at all. You know,

with the excitement behind ABS 2011, I cannot help but think about my own personal practice and where I am with Schwea Dermatology. I mean, as I

Schwea Dermatology. I mean, as I mentioned, we're talking about slightly under 200 practices coast to coast.

We're the second largest dermatology group in the country. You know, we have over 2 million patient visits every year. Roughly 10% of people coming in

year. Roughly 10% of people coming in coming for hair thinning. I can only imagine the commercial market we're going to have once ABS 2011 comes onto the market. So we recognize uh what role

the market. So we recognize uh what role ABS 2011 can play in in our you know huge dermatology practice. Uh but it'd be nice to now hear something about the commercial development of this product.

And with that I'll pass it on to Mike and Zach.

>> Good morning everyone. My name is Mike Jafar and excited to be here and appreciate the AppSite team for for inviting me. Um, I've built my entire

inviting me. Um, I've built my entire career and been fortunate to be around great people and great brands in this cross-section of of medicine and and

aesthetics. I've had a chance to scale

aesthetics. I've had a chance to scale uh build from zero to one uh acquire and just be part of an organization at the time called Now Avy uh that owned many

of these assets like Botox and Cool Sculpting and and Juvéderm. uh also was the chief commercial officer for a public company called Eveis who had a wonderful product and frankly the first

product to compete against Botox called Javo and took that company from zero to a few hundred million in revenue as as we scaled the company at the time that uh we spent at Allergan developing the

latis business we started to learn a lot about hair right and hypertrois was a thing and we started to talk to tririccologists and dermatologists that really understood hair what was really

hard at the time was to find an asset that that impacted so many people in America. Um, and that that drove this

America. Um, and that that drove this definition of the last frontier that we were always looking for, at least at my time and hour. If you look at just hair

loss in general, nearly a third of Americans are impacted by by this. Uh,

and it has a massive psychological impact. Clearly, it has a visible

impact. Clearly, it has a visible impact. It's one of the few things that

impact. It's one of the few things that impacts both men and women, kind of akin to weight loss. So just the idea to address this from a true scientific

standpoint with a novelty product and a novelty target I think has such mass commercial appeal. The limitation and

commercial appeal. The limitation and why this category has been so hard has been driven by the lack of efficacy frankly andor an experience that many don't want to go through. So if you look

at just the consumer base today and what they're willing to do, clearly they're willing to be on topical meds for the rest of their life, systemic products.

Um uh they're interested in surgery. Some are flying to Turkey. I

in surgery. Some are flying to Turkey. I

mean this is this is such a profound need in the marketplace. Uh but

unfortunately it all comes with massive drawbacks. whether it's systemic side

drawbacks. whether it's systemic side effect or the experience of uh of a hair transplant, the stigma behind surgery.

Um even despite going to the far, you know, the greatest lengths of of surgery, you still have to maintain and and be on uh these topical drugs that many people just don't want to be. So,

it's just been a high burden um for for I'd say decent or mediocre results at best. Uh and the opportunity here is to

best. Uh and the opportunity here is to reframe this. If you look at what

reframe this. If you look at what patients and clinicians are seeking for for just better treatments, right, significant hair growth, durability,

safety, especially around side effects, um, and then conveniency. The idea of taking daily administration of drugs that may have an impact on sexual dysfunction. It may have an impact on a

dysfunction. It may have an impact on a host of things systemically is just not appealing to the masses, which is why I feel like there's there's a greater cohort sitting on the sideline looking

for something like Absai's project that we'll discuss today. So, if you look at the ABS 2011 target product profile, the the opportunity to deliver a blockbuster drug if if the following tenants are

met, I think is is is the exciting part.

Right now, right now we sit on oral minoxidil as the gold standard. So ABS

2011 has to be greater than oral minoxidil when it comes to hair growth.

Durability is critical. The idea of taking something and however it's administered lasting for a few years is clearly uh an unmet need and and a

driver of growth. Safety and efficacy is a non-negotiable, right? Um and then lastly a a subcutaneous injection once twice you know three times over the

course of of the year lasting for two to three years would be would be ideal.

So if you look at the ABS 21 target product profile as it compares to what's out in the marketplace, minoxidil, finestide topicals orals PRP

it is the only target product profile that exists in the marketplace that allows you a a few interactions with with long range durability. Taking a few

thousand pills over the course of three years is not that exciting for people, right? uh going in for PRP four to five

right? uh going in for PRP four to five times a year every year and getting an injection upwards of 30 to 40 times on your scalp is not terribly appealing

which is why you see a massive drop off rate when it comes to PRP. So from an efficacy standpoint here's what the market has has come to call it trade-off. You got convenience and

trade-off. You got convenience and comfort on one side and then you have performance or or call it outcomes and growth on the other side. Ideally, you

want to be in the top right. Super

convenient, extremely comfortable interaction with any product with tremendous duration and/or outcome.

Right? That is that is the target product profile design. That's where you want to be. Unfortunately, the only option today for most consumers is

either uncomfortable, high frequency, or minimal outcome. I I feel like uh at my

minimal outcome. I I feel like uh at my time at Allergan, we always used to say body contouring was the next uh frontier and then came along cool sculpting now was impic uh but in the background the

last frontier truly was hair and and it's so wonderful to be part of this project with Sean and Zach and the Absai team. So, thank you for having me.

team. So, thank you for having me.

>> Hi, I'm Zach Jonison. I'm the CFO and chief business officer at ABSAI. Today,

I'm excited to share some results from our market research. We started this process by interviewing both CL clinic clinicians as well as patients and then

commissioned a consumer research survey in the fall of this year. This survey

included 610 participants about evenly split between males and females. They

were all US adults 25 to 59 years old with an income exceeding $75,000 a year including some disposable income. and

all of the participants were experiencing and bothered by hair loss or hair thinning. The objectives of this survey were to assess attitudes about

hair loss as well as as well as survey the psychosocial impacts of hair loss.

We also looked at consumers sentiments around current standard of care and we explored interest in the ABS 2011 target product profile including willingness to

pay premium for such a TPP. So, we're

going to share a few results from this study. To level set, we asked patients

study. To level set, we asked patients about the impacts of their hair loss on their psychological well-being. What we

found is 80% of men and 81% of women registered strong negative psychological impacts from their hair loss.

principally feeling less confident, feeling like they looked less attractive, and also feeling like they looked older than their actual age, and generally feeling self-conscious in social situations.

These results correspond to the patient testimonials you heard earlier today from Kelly and Landon and are a strong motivator for why these patients seek treatment. We also asked respondents

treatment. We also asked respondents about their interest level in the ABS 2011 target product profile. And here we see a vast majority of both males and

women were highly interested. In fact,

87% of men surveyed said they were extremely or very likely to ask a health care professional about procuring the ABS 2011 product if it were available.

Similarly, 69% of women said that they were extremely or very likely to seek out ABS 2011 from a healthcare professional. We also wanted to evaluate

professional. We also wanted to evaluate the interest level of patients who are currently taking a standard of care therapy in ABS 2011. And here the results are even more exciting. Patients

that are on a current standard of care therapy were even more interested in contacting a health care professional about ABS 2011. For example,

90% of men currently taking topical minoxidil said they were extremely or very likely to contact a health care professional about ABS 2011.

92% of men currently taking oral minoxidil said they were likely or very likely or extremely likely to contact an

HCP about ABS 2011. And finally, 97% of men undergoing in-office procedures such as PRP or hair transplantation said they

were extremely or very likely to contact an HCP about ABS 2011.

Similarly, with women, we see 76% of women who are currently taking topical minoxidil said that they were extremely or very likely to contact a health care

professional about ABS 2011. That number

goes to 89% of women who are taking oral minoxidil. And finally, 88% of women who

minoxidil. And finally, 88% of women who are undergoing inoff procedures such as PRP or hair transplantation said they were extremely or very likely to contact

a healthcare professional about procuring ABS 2011. Now, these results undersc underscore two important points.

First, the standard of care isn't cutting it. Patients are dissat

cutting it. Patients are dissat dissatisfied with current treatment options. and secondly the strong

options. and secondly the strong interest in the TPP that ABS 2011 offers. We further asked respondents

offers. We further asked respondents about their interest in using ABS2N as firstline therapy. And here the results

firstline therapy. And here the results are very exciting. 37% of men said they would try ABS 201 as their first course

of therapy to treat Aga and 36% of women said they would try it as a first line.

The key takeaways from our consumer research, including the survey we just discussed, are number one, we confirmed the significant unmet need that exists today, which is driven by the

psychological impacts from hair loss.

Number two, the overall high level of interest in ABS 2011 and the potential for it to become firstline therapy for a significant share of both male and

female AGA consumers. And number three, although we did not discuss the results from the questions pertaining to pricing in our survey, we found that there was a significant share of men and women

respondents who were willing to pay a premium for the ABS 2011 target product profile. Using data from our consumer

profile. Using data from our consumer survey as well as demographic data, we were able to construct a classic patient treatment funnel. Here at the top of the

treatment funnel. Here at the top of the funnel, we start with the total estimated AGA population in the US of 80 million. We then cut the funnel and

million. We then cut the funnel and according to income. Here we're looking at a the AGA population that would have an income greater than $75,000 a year

and be within the age brackets 17 to 69 years old. That brings the funnel to an

years old. That brings the funnel to an estimated 39 million.

Then we further cut the funnel according to the AGA population that is concerned and motivated about treating their hair loss. That brings the funnel to an

loss. That brings the funnel to an estimated 26 million US consumers. The

next cut of the funnel considers the interest level in the target product profile of ABS 2011 based on our consumer market research survey. This

brings the funnel to an estimated 22 to 24 million AGA consumers. The final cut of the funnel is constrained to AGA consumers with the highest interest in

the TPP and willing to pay premium pricing based on our survey. This brings

the funnel to an estimated 15 to 18 million patients. Now, if we assume two

million patients. Now, if we assume two to three years of durability of the ABS 2011 treatment, this would imply 5 to 9

million patients are treated each year.

At that level of treatment, we estimate a total available market in the US of greater than$2 billion and a potential TAM of greater than 40

billion globally.

We're also pleased to see that the go to market channels are already in place.

80% of consumers that seek hair treatments already go to our target market channels, principally dermatologists, med spas, and plastic

surgeons. So, as we think about a

surgeons. So, as we think about a potential FDA approval in 2029 or 2030, we believe we're well positioned to ramp into this market, there are currently

over 30,000 of these locations when you consider dermatologists, met spas, and plastic surgeon offices across the US alone. More broadly, we believe we have

alone. More broadly, we believe we have a strong strategy to capture and expand the ABS 2011 total available market.

We're starting from a position of strength. There's a massive motivated

strength. There's a massive motivated patient population with high unmet need and with high interest in the ABS 2011 TPP based on our survey results. There's

also a robust practitioner market channel already in place encompassing the derm offices, plastic surgeons, and metapas.

And as we think about going forward once the product is approved, we'll be focused on creating viral awareness and direct patient engagement. We'll also be looking to leverage our first mover

advantage to create an iconic brand to further protect and grow our market share. Finally, longer term, we look to

share. Finally, longer term, we look to expand the market by going direct to consumer. We're excited to leverage both

consumer. We're excited to leverage both the strategy and the market infrastructure built by the Glip One players.

And when we look at that playbook postmarket, we'll be focused on creating viral awareness of ABS 2011 that can drive more patients to clinicians, hence

driving more demand and more revenue. We

will also be looking to build direct patient engagement which can enable further expansion of the market in a direct to consumer fashion. Altogether,

we're very excited to advance ABS 2011 through clinical development towards approval. We believe this therapy can be

approval. We believe this therapy can be category defining and address the significant unmet need that exists in the AGA population today. And with that,

I'm happy to turn it back over to Shawn.

Thank you, Mike and Zach. And a huge thank you to Dr. Rossy, Professor Paw, Professor Sinclair, and Dr. Goldberg for sharing their time and expertise with us

today. I want to close by connecting the

today. I want to close by connecting the dots on what we've heard over the past hour. We started this session grounded

hour. We started this session grounded in the reality of the patient experience. And I want to sincerely

experience. And I want to sincerely thank Kelly and Landon for being so open with their personal stories.

Hearing Landon, an elite athlete and a soccer legend and icon, talk about his hair loss experience and how that's impacted him really drives home the

point that Dr. Rossi made earlier today that this is not just a cosmetic issue.

It deeply is tied to identity and our mental well-being. Regardless of who you

mental well-being. Regardless of who you are or what you've achieved from that foundation, we went deep into the science. We saw the biology with

science. We saw the biology with Professor Paws and Professor Sinclair validating the prolactin receptor mechanism as a master switch of hair

regrowth. We saw how ABS 2011 is

regrowth. We saw how ABS 2011 is uniquely engineered to unlock that pathway. And finally, Dr. Goldberg,

pathway. And finally, Dr. Goldberg, Mike, and Zach made the commercial reality clear. The bar for success is

reality clear. The bar for success is defined, and the market opportunity is effectively uncapped for a drug that delivers durable efficacy with a clean

safety profile. For Absai, ABS 2011

safety profile. For Absai, ABS 2011 represents exactly what we set out to do as a company. We used our generative AI platform to identify a high value

biological target and design a best-in-class biologic to address it faster and more precisely than traditional methods allow. We are

incredibly excited that we have started the trial this month and already have enrolled our first cohort. With the

protocol Dr. Sinclair and Dennis outlined, we have a streamlined, efficient path to a proof of concept. We

anticipate sharing an interim efficacy readout in the second half of next year.

We look forward to updating you as we progress through the clinic and ultimately to sharing the data we believe will transform the standard of

care for patients like Kelly and Landon and millions of others.

Thank you for joining us today and thank you for your continued support of ABSI.

For the Q&A section of today's session, we'll be utilizing the raised hand feature. If you'd like to ask a

feature. If you'd like to ask a question, click on the raise hand button at the bottom of the screen. Once

prompted, please unmute yourself and begin with your question. As a reminder, we ask that you stick to one question and one followup. We'll now pause a

moment to assemble the queue. Thank you.

Our first question comes from Van Vamil Devon with Guggenheim. Your line is open. Please feel free to unmute and ask

open. Please feel free to unmute and ask your question.

Mel, please unmute your line and that's >> sorry about that. Can you hear me now?

>> Okay.

>> Yeah, we can hear you.

>> Okay. Sorry about that. Um, so I just had a couple questions more on sort of the commercial side of things and you mentioned the sort of pay for performance that people be willing to pay for and I'm I'm curious just given

the nature of this product and I guess you'd be paying upfront and then getting the benefit over time would there be are you thinking about some sort of almost like a valuebased pricing where people

pay upfront you and then it's sort of dependent on how they respond is kind of what they're paying. I'm just trying to get a sense because I'm assuming it' be a a relatively large upfront cost that people would be having to put up for

that. And then the other question I had

that. And then the other question I had was just around some of the market research which was very helpful. So

appreciate you sharing that. I noticed

there was like a little bit of a difference. I think you know very strong

difference. I think you know very strong interest from men and women but for men it was like 90%. For women I think the interest in talking to the doctor about it was around 70%. So a little bit of a difference. I'm just curious if anything

difference. I'm just curious if anything you saw in the research that's showing, you know, differences in how men and women are reacting to the the potential

target profile here. Thank you.

>> Yeah, thank you Voml. I I think one of the things that uh came as no surprise to us as we had talked with with Kwells was just uh the immense impact that this

has on both men and women. uh men and women look at it, you know, slightly uh differently. One of the things that, you

differently. One of the things that, you know, women uh really care a lot about is is seeing the the hair in the drain uh when they shower uh versus men, it's

uh you know, losing uh the the hair in the uh in the front area of the scalp as well as um just wanting to be able to to regrow that. And you know, in regards to

regrow that. And you know, in regards to the commercial side of things, I'll hand that over to uh Zach and and Mike to to get their perspective on that. Zach, you

want to start off?

>> Sure. Thanks. Thanks, Sean. So Vanna,

one one other point when you dig into the numbers of male versus female in the consumer research study, one thing that's important to point out is if you look at women that are actually already

taking a standard care treatment, those numbers are very similar to men with respect to their interest level and ABS 2011 and we also see very similar level

of u excitement about using ABS 2011 if it were available as first line. So we

think the survey data is tremendously strong supporting the TPP and how well we see this is going to be in the marketplace. As to your question about

marketplace. As to your question about uh financing plans and how you might structure payment uh for ABS 21, I I think it's too early for us to really uh go through that. I will say we do

believe uh longer term there will be ways to do financing plans around this and and spread out payments for for patients. But in our survey, we really

patients. But in our survey, we really didn't uh test test those assumptions and whether that would further expand interest. We really presented it as a in

interest. We really presented it as a in the pricing portions as a upfront cost.

Um and I think patients were able to compare that to what it would cost for other standard of care and also compare what the efficacy and durability would be relative to other standard of care.

>> Okay.

>> If you would like to comment as well.

>> Yeah, happy to. happy to compliment this. Keep in mind that the consumer

this. Keep in mind that the consumer today, if they're going in for CO2 and the physicians on the phone can speak to this or body contouring, they're paying

for something that has prolong effect, not immediate effect. And so I think the mindset of the consumer to to exchange money for a procedure and then watch the

effect happen over time is not a foreign concept in our category. It happens

daily. If anything, uh you would probably ask for a refund after a CO2 treatment because the first three to four weeks are frankly um the experience is not not optimal. Um same thing with

body contouring when when we're managing the body uh body contouring cool sculpting business, you would take several thousands of dollars and you would tell the consumer that the effect will happen over time. So the mindset of

the consumer is already there.

>> Sean, if I can comment at this point.

>> Yes, absolutely. Go for it, Dr. Billberg.

>> So, you know, Vamu, you and I have talked about this a little bit as well before. Um, you know, two things. One,

before. Um, you know, two things. One,

patients coming in for PRP injections, you know, which is really our standard of care now. Forget about the fact that they have to get the phabbotomy of their arm and injected multiple times in their scalp and it's a pain in the neck for

them. You know, they're paying I mean,

them. You know, they're paying I mean, in the Midwest maybe $1,000 a treatment.

You know, I'm in New York and New Jersey it's 2,000 sometimes $3,000 a treatment.

They're paying good good money right now for a treatment that does very very little. And so it's not hard to

little. And so it's not hard to extrapolate from that to figure that they're going to pay for this. The other

comment I want to make is um you know I I listening to some of the data out there you know for someone like me who runs a very strong FDA research program on on multiple treatments for hair um

you know some 30 I think the numbers I heard 37 38% of people if offered uh ABS 2011 um would jump to it. And I find that number remarkably high because this

is a drug that's not on the market at all. You know, we have so much trouble

all. You know, we have so much trouble getting people into any of our studies because, you know, it's it's it's new and and our success rate, you know, some of the other things we do, uh, getting

people in studies is really under 10%.

So, the fact that 37 38% of people if given the option to use ABS 2011, um, would do would use it tells you how how difficult this market is right now.

Okay, thanks for those thoughts. I

appreciate it.

>> Our next question comes from Brendan Smith with TD Cohen. Please unmute your line and ask your question.

>> Hi, can you hear me?

Hi, this is uh Jackie on for Brendan. As

>> Hey.

>> Hey. As as much as I'd love to ask uh Landon Donovan a question or two, I'll just uh stick with just one for you guys.

>> And uh I know you've mentioned that there's plenty of room for multiple players within the AGA space and given the size and the unmet need, and you've demonstrated that great today. That

said, I'd be remiss to not bring up Cosmoarma's recent phase 3 data which demonstrated significant improvements in their hair growth over placebo.

Obviously, these are very different MOAs and you've also spoken to the DHT and androgen receptor targets today as well.

But assuming does make it to market, could you walk us through what the patient split might be? You know, which patient types are more likely to choose ABS 2011 over a topical solution and

sort of what the dynamics may be around that competitive lineup.

>> Yeah, it's a great question. uh if you look at the Cosmo data, I'll hand it over to both Dennis and and the Kwell's on the line to speak to this. Uh but the uh percent increase was to to baseline

and if you you know compare that to uh minoxido, it's right in line with minoxido. Uh so it doesn't seem like

minoxido. Uh so it doesn't seem like there is uh much of a benefit compared to uh current standard of of care. But

uh Dennis uh and you know, Professor Sinclair, Dr. Goldberg, and Dr. Please feel free to uh chime in as well.

>> Yeah, hi Sean happy to do so. Um as Sean mentioned um it seems to be rather a safer option as finesser than deserite from a topical administration and this

500% or 300% sounds in initially very very um significant but it's if you average it with a high variability across the tri approximately threefold

which compares to minoxidil effect. So,

but um basically we we see that um as Sean outlined also um as potential complimentary >> does any of the ch

that I think what it's the classicalone seems to be comparable to is the topical minoxidol rather than the oral it's

weak and from a price compar of view it's not something I would be in have legs we'll have to wait and see the actual head

describing it as a percentage is a bit >> yeah the the the Cosmo data I mean if you look at it you know the the idea behind this is to have a topical form of finestide if you will without the

potential side effects but it's really looked as an alternative to topical minoxidil. I look at it as an adjunctive

minoxidil. I look at it as an adjunctive treatment. I think there there will be

treatment. I think there there will be other adjunctive treatments as well, but I I don't see this in the same place as ABS 2011.

And we know from other topicals that compliance is such a limiting factor of daily use and such and patients are just not great with compliance on topicals.

And for most of us, we're treating hair in a multimodality fashion. So, you

know, while we have our systemic medications, we also supplement with topicals if if the patient is even willing to do topicals.

>> That's super helpful. Thank you so much.

>> Dr. Sinclair, do we have you back online? You were uh cutting in and out

online? You were uh cutting in and out there.

>> Yeah, I think uh it had jumped on the Wi-Fi, so I think I'm back now. I can

hear you and hopefully >> Perfect.

>> Do you maybe just uh want to repeat what what you said? I think you were cutting in and it out there.

>> So, so what I was saying is that my interpretation of the Klescottone data is that it was a a comparison to the topical minoxid, not the oral minoxidol.

The way they've presented the data as a percentage increase isn't really comparable to other forms. It should be presented as an absolute hair count change. And so I'm very skeptical that

change. And so I'm very skeptical that clasotone is going to be an effective treatment and it certainly wouldn't be something I would personally invest in.

And I think it's it's uh it's going to have uh hairs on it, so to speak.

>> Great. Thank you.

>> Our next question comes from Gil Bloom with NEM. Please unmute your line and

with NEM. Please unmute your line and ask your question.

Hear me?

Yeah, we can hear you go.

>> All right. So, just a couple of quick points from us. Um,

considering there is this, you know, study was conducted in in endometriosis, is there any anecdotal evidence from that study of hair regrowth in the women

treated? And maybe a more you know

treated? And maybe a more you know general question as to the study data cadence.

Will we have any reports out of the SAD portion of the study ahead of the larger uh data set in the second half? Thank

you.

>> Great. I can answer that that first question. So we do plan to have a safety

question. So we do plan to have a safety readout on the SAD uh prior to the 13week efficacy readout in the second half. Uh so uh be on the lookout uh for

half. Uh so uh be on the lookout uh for that. And uh with regards to the first

that. And uh with regards to the first question uh Dennis and and I'll I'll hand that over over to you.

>> Yeah, happy to take the question. So

unfortunately um there is no information on the androgenetic phenotype in in women reported in the endomaterials trial. We were also looking forward to

trial. We were also looking forward to see some anecdotal outcome but um we will have to wait for our trials to see an effect.

>> Thank you.

>> Our next question comes from Brian Chang with JP Morgan. Please unmute your line and ask your question.

Uh, hey D. Can you hear me?

>> Yep. Loud and clear. Brian.

>> Uh, well, thanks for taking our questions here. Uh, a couple from us.

questions here. Uh, a couple from us.

Um, just want to pick your brain a bit on the setup for the phase one 2A trial.

um what do you want to see across the three doses um in the maths portion that you have selected um for hair counts and

also hair with uh and then we have a quick followup. Thank you.

quick followup. Thank you.

>> Yeah, it's a great question. Uh so the PPP slide that Zach went over what we're looking to to achieve is uh you know at

the higher end of or minoxidil you know potentially uh up to what you see in in a hair transplant uh we see that as

ultimately being a win uh in terms of uh total uh area hair count and uh Dennis you know please feel free and as well as

uh Dr. Sinclair uh to give your perspective on this as well.

>> Yeah, absolutely. Um maybe also tying it back to the topic which Rodney touched upon with receptor occupancy. So the

doses have been selected in a way that we can see um a dose response relationship um to really then define for the later clinical development um

the efficacious dose we want to then further test into the bigger cohorts.

Rodney, do you want to add something to that?

>> So, I suppose as a comparison, oral finasteride grows around about 20 hairs per cime

foam grows about 16 hair per cm. The the

lotion's a little bit more than that.

The oral minoxidil is looking to grow around about 30 to 40 hairs per cime. a

hair transplant somewhere between about 25 and 30 hairs per centimeter. You

can't pack them much closer than that.

So, I think we want to be in the range of north of 30, but ideally north of 40 hairs per centimeter. Then you'd have a a very very strong uh market uh

comparison. And then the other thing of

comparison. And then the other thing of course is there's the hint in the macak monkey studies of longevity of the response. If you can actually

response. If you can actually demonstrate that in the studies, and that'll take a little bit longer, of course, if you can actually generate a sustained response after they've completed the dosing, then that's also going to make it attractive for people

who want to move away from having to take a daily.

And then if if I can just add one more um just on the subq versus IV dose uh formulation here, how should we think of

the subq dose range um in relationship to um the IV doses that you have selected? Thank you.

selected? Thank you.

>> That that's a really great question. So

the IV dose is mainly to establish really safety and tolerability where you have a really 100% by availability. So

you really establish um this this uh fundamental foundation for your clinical development. And with regard to the subq

development. And with regard to the subq dozing um there this is also the later intended commercial route of administration where then we will um see

also the profile of bioavailability after subcqure administration and then together with the PK profile which we obtain we can then determine uh at which

dose we see really um the best hair growth efficacy uh in combination also with the dozing interval down the line.

Yeah, and we are currently at 200 MIGs per mill and that will be the uh commercial uh subq formulation. Uh so

that will be tested in in the MAD and uh what we saw in the NHP was greater than 90% bioavailability uh for that subq formulation.

>> Great. Thank you guys.

>> Our next question comes from Devonjanna Chadi at Jones Research. Please unmute

your line and ask your question.

>> Hi.

>> Hi. Do you guys hear me?

>> Uh thanks for the exciting presentation.

So uh can you please confirm if the Xvivo experiments were performed on hair follicles from healthy male donors and uh if so how do you think the uh

findings would translate into um like you know patients with established AGA?

And I have a commercial uh followup.

Yeah, absolutely. Uh, professor uh pause, do you want to uh answer that?

>> Yeah, actually that's a brilliant question. Um, so when we um do these

question. Um, so when we um do these scalp skin organ cultures, they have to be done in anonymized fashion and uh so we're not allowed to know anything about

the skin other than where it is from age and sex. But it was all from the

and sex. But it was all from the temporal frontal region. And if you look carefully at the gentleman here in this zoom call, they all have androgenetic

alopecia in the um frontal temporal region. So the likelihood that the three

region. So the likelihood that the three donors we investigated um all had that too was extremely high.

But you're absolutely right. We can't

100% guarantee this. So in in theory they were healthy because we are not allowed to know whether they had a does it answer your question?

>> Yes. Thank you. And uh maybe thinking about the >> professor professor I was just going to add one other piece. uh we we didn't share this this data but I think it'd be

good for you to to speak to it is actually in each of those patients uh what we saw from a prolactin receptor um profile and what that what that looked like.

>> Yeah. So there there were also interindividual differences in the prolle receptor expression profile which is to be expected. Basically every

hormone receptor uh that you look at show individual variations. And yet

despite these uh substantial prolact receptor um expression differences between these three donors we looked at uh we had significant and reproducible

responses throughout these three donors.

Now three donors that's nothing compared to the hundreds of patients that are now going to clinical trial. Right? But

that's what you can do at the preclinical level. But for um since we

preclinical level. But for um since we have run these pre-clinical trials for a very long time uh if we find such reproducible uh um results within three

different donors for us this is very very encouraging and uh remember that um what we're looking as is the human target organ itself. It's not some mouse

model not some monkey. We are looking at real frontal temporal human scalp skin.

And to see such reproducible data is actually at the level of preclinical research highly encouraging.

>> Great. Thanks for this insight.

>> And are there any additional uh you know hair loss conditions where you think um modulating the prolactin signal could offer therapeutic benefit outside of AGA?

>> Yeah.

>> Yeah.

>> Go for it, Dennis.

Oh, that that's another great question.

Of course, we are also exploring the the space where this mechanism could hold true. Another area could be of course

true. Another area could be of course alopecia ariata based on what also professor Paul mentioned the role on productin on immune modulation. Um so

we're conducting pre-clinical studies and we'll we'll of course explore different different indications but also uh dermatology areas. Maybe Anthony or Mike want to share um some some thoughts

there too. Um but I just wanted also to

there too. Um but I just wanted also to briefly mention that um with the donors um even if one of the donors or two of the donors might not have HA um they are

really um promising because that also shows you that this mechanism works in healthy skin and will likely most work even better when prolactin is a driver

of of this phenotype.

>> Very helpful. Thanks for commenting the line.

>> Do do you want to >> Yeah. Yeah, if I if I can add

>> Yeah. Yeah, if I if I can add >> you want to mention that that that the skin Yeah. Go.

skin Yeah. Go.

>> Yeah. So, so um additional indications in skin. Um if you remember the stem

in skin. Um if you remember the stem cell data we showed u so so as you know there are very nasty hair loss disorders which actually increasing in in

incidence and prevalence particularly frontal fibros alopeesia and these these hair loss disorders are caused by depletion of hair follicical epithelial

stem cells. Um so if you now have a new

stem cells. Um so if you now have a new antibbody that um uh protects these uh hair stem cells from cell death uh and

um keeps them in a better position to produce daughter cells as this antibbody seems to be doing. Um you might actually have uh a new therapy that could be at

least used as an agent therapy in this very nasty form of helosto fibros alopecia. many patients affected um to

alopecia. many patients affected um to whom we have fairly little to offer these days.

>> If I might chime in also another indication is going to be tiloggen of fluvium. Oh absolutely because that's

fluvium. Oh absolutely because that's what our data support right that antigen gets prolonged anything that prolongs antigen will be a wonderful treatment uh

to suppress tilogen influ if the durability of the effect is as long um as as initial data seem to suggest um then that would be wonderful news. So

with one or two shots of the antibbody, you could have a very long-lasting tigen fluin um reduction and that is often the first uh um symptom that that brings the

uh the patient to the dermatologist that they find this increased hair shaft shedding and increased hair shaft shedding that is tagglio.

If I can, you know, extrapolate that one step further, we're seeing so many people now on the GLP-1 agonist coming in also with hair loss and whether that's a tilogen of what exactly is

going on there, I don't think we know.

But to me, I I know as this drug comes to market, when those people start coming in complaining about volume loss, lack skin, they're often complaining about hair thinning as well, and you know, they're going to go right on this

injection.

>> Very true. 10 to 20% actually of these patients on the drug complaining about telogenium. Yeah.

telogenium. Yeah.

>> And and like frontal fibrosin there are other scarring alipcas that are you know really have a posity of any treatments available. So it would be amazing to

available. So it would be amazing to actually you know try this in that in those >> great uh thanks for all the additional color very useful context.

Thank you. Our next question comes from Morgan Greger with Morgan Stanley.

Please unmute your line and ask your question.

>> Hi everyone, thanks. I'm calling in for Sean Lawman. Um, so we've seen in

Sean Lawman. Um, so we've seen in preclinical studies for ABS 2011 potential repigmentation effects too.

How could that present potential upside for ABS 2011 in this market?

Yeah, it's a it's a great question and uh actually that's a piece of data that was was not shown but we did generate which was very promising. Uh professor

pause do you want to talk a little bit about the the melanin uh data that we got in from the uh Xva?

>> Well so so the verdict on that is still out what the pigmentation effect in a hair cycle independent manner is but there seems to be a stimulation of the hair follicle pigmentaryary unit. Um one

thing one needs to keep in mind whenever whenever a gray or white hair follicle gets repigmented that can only happen in anogen during the growth phase. So it's

an absolute prerequisite for any kind of repigmentation of gray hair that the follicle stays longer in anogen and reactivates its pigmentaryary unit. Um

and the initial data that that we have from these preclininal preclinical trials uh would suggest that even that the antibbody might be able to do but we

have to shore up this evidence to be more most more certain about that.

>> Right. Thank you.

>> Our next question comes from Charles Wallace at HC Wayright. Please unmute

your line and ask your question.

Hi, uh, thanks for a great presentation.

Um, and, uh, a little bit of color if I may on the headline phase 2A design. Um,

regarding later clinical development, would you need to do additional tri or what additional trials would you need to do? Um, would you uh, go into a phase 2b

do? Um, would you uh, go into a phase 2b or directly into a phase three? And then

also, is there precedence to keep males and females in separate cohorts or even separate studies? Thanks.

separate studies? Thanks.

>> Yeah, it's a it's a great question. Uh

so in this current study that that we're doing, we we do have uh females uh in in the SAD uh to enable uh the phase 2 study uh that'll start in in Q4 and

endometriosis. Uh and we do have

endometriosis. Uh and we do have optional cohort uh in uh the the MAD uh that we're we're planning on on filling.

uh and the the depending on how the the trial goes uh you know our plan would be to uh have a registrational uh trial after this. Dennis I don't know if you

after this. Dennis I don't know if you have anything Dennis or Zach if you have anything else to to add regarding uh the plan there.

>> Sure. happy happy to expand on what you already perfectly alluded to is um that uh if everything goes well especially when we're looking at the male participants um the the additional

pieces which are then missing is a long-term um uh safety database um so you could envision directly proceeding in a combined phase 23 study design to

have an accelerated um clinical development setting.

>> Great. And then a followup if I may. Um

so on the on the uh proof of concept data that's coming out um what differences should we expect to see between the 13 weeks and the 26 weeks

and then also on this um would we get an any idea of the potential repigmentation uh from these readouts? Thanks

>> uh Dennis and then uh Dr. Sinclair.

Yeah, sure. Happy happy uh to give a first uh stab at it and hand it over to Rod. Um so basically when you look at

Rod. Um so basically when you look at classical hair regrowth trial, each mechanism has a different uh rate of how the hair growth. Um some are steady, some plateau. Um so of course we

some plateau. Um so of course we anticipate uh as you have seen from the NHP data that we have a continuous growth but u we are looking forward to

see initial um uh differences at 13 weeks which can then guide our um next clinical um steps but of course we anticipate that at 26 week uh the amount

of hairs grown and delta will then even be bigger than compared um to plus able but um rod um maybe you have also an additional

So, >> sure. Um, I think that the trajectory of

>> sure. Um, I think that the trajectory of growth is going to be very similar to what we've seen with minoxidil. So, with

the finasteride where you work from the bottom up from the hair bulb up the hair follicle, the peak improvement in hair count was about 12 months. Whereas with

the minoxidil, the peak improvement in hair count was around about 16 weeks.

And a lot of the minoxal trials have been uh focused on 16 weeks. I know

Verodmix recently released their phase 2 data and they showed about um I think it was about 30 hairs per centimeter at 2 months and 40 hairs at 4 months. Um

that's similar to what we've seen with the sublingual minoxidal data which is uh not yet publicly available. Um, and

so I think that's the sort of trajectory that we would be hoping to see with a prolactin. With regards to hair color,

prolactin. With regards to hair color, this is probably the first time that we're looking at hair repigmentation

through a clinical trial. We originally

did studies in twins in gray hair. And

it was very hard to do because when we were just looking at people from a distance like through the zoom, the perception of graying of the hair is very much influenced by hair length. And

so I know that if I let my hair grow long, it goes a bit dark and then I get a haircut, it suddenly goes all gray.

And so now we're doing the hair color through photo triagram. So we're going to get a much more accurate reading and it's going to happen much quicker. And

uh and I think this is probably to my knowledge one of the first studies we were actually investigating hair color.

We've seen with minoxidil some very soft observations that it delays graying but it's not as significant in terms of reversing gray and I can say that from personal experience having been on oral

minoxil for over 12 years and I've gone very gray. So minoxidil doesn't do it.

very gray. So minoxidil doesn't do it.

will be interested to see whether the the the um the EPSI molecule does.

>> Great. Yeah, I know. Uh my mom would be one of your first customers if if that's the case. Uh

the case. Uh >> well, the big the big custom for gray hair is Southeast Asia. So whilst it's universal amongst women on this planet

that they don't like gray hair, gray hair is very largely tolerated by by men in in Western societies. But in

Southeast Asia, gray hair has got very low acceptability. And so all the men in

low acceptability. And so all the men in Southeast Asia, that's a that's a huge market.

>> And in the Arab countries as well, >> maybe it's not >> maybe it's noteworthy that uh we're all excited about repigmentation. However,

this is not baked into our case. I think

we should we should point that out at this point.

>> Great. Thank you, guys. Our

last question will come from Annalie with Truist. Please unmute your line and

with Truist. Please unmute your line and ask your question.

>> Hi, can you guys hear me?

>> Yep.

>> Um, hi, this is Anna um on for Truist on for Crypa. Sorry. Thanks for the

for Crypa. Sorry. Thanks for the question. Um, for Dr. Sinclair, uh, one

question. Um, for Dr. Sinclair, uh, one question besides the dose selection, could you also talk about any key trial design differences between the HMI115

hope trial and the headline trial? And I

have a followup.

So the hope trial was an intravenous study. This is a subcutaneous this is

study. This is a subcutaneous this is sort of staged in in two phases. The the

hope study was a was an open label study. Uh so all the patients received

study. Uh so all the patients received active medication. Um this is a a

active medication. Um this is a a subcutaneous study. There's um different

subcutaneous study. There's um different dosing cohorts. There's men and women. I

dosing cohorts. There's men and women. I

suppose the the hope study also had male men and women as well. Um but this is a much larger study. The in terms of the primary endpoint of the study, it still

centers around target area hair count.

Secondary endpoints are target area hair width um and global photography and patient reported outcome measures. But

everything really centers around the target area count pretty much all the hair studies. All the others are are

hair studies. All the others are are nice to haves rather than must haves. we

really want to see significant um improvement in the in the target hair count of nonvellis hairs.

>> Yeah. And and to expand on on what Rodney mentioned also um we have also included now target area head darkening although as as rightfully Andreas mentioned we have not baked it into the

case and we are still looking into this phenomena too. And then uh we are

phenomena too. And then uh we are exploring way higher doses for example in the clinical trial to really address this receptor occupancy and efficacy

topic than the hope medicine um study.

So we really believe that with the current clinical design we will be able to um uh bring the best out of this mechanism.

Great.

>> Um and um any expectations for kind of that safety sad readout besides kind of looking at halflife any potential safety concerns? I know there's like some

concerns? I know there's like some theoretical concerns of prolactin suppression um with like immune bone loss anything like that.

Yeah, Dennis, do you want to speak to that and uh Dr. Sinclair after that?

>> Yeah, sure. Happy to do so. Um, so as you have heard from Andreas initially, so um this u this mechanism is really one one spectacular where we have the

human genetics showing really a favorable um safety profile. So the

affected individuals are healthy. We

also have um phenomenal toxicology data so far from a preclinical toxicology. So

where you have really to test high doses of uh of the drug in in NHPS and then you also have the precedence of of antiprotectin receptor inhibition in

clinical trials where also at very high doses um the participants showed no adverse events. So all taken together um

adverse events. So all taken together um we we are pretty confident moving forward. Nevertheless, we have of always

forward. Nevertheless, we have of always of course the safety of the participant as our highest priority and we will record uh any any observations

throughout the clinical trial and also right will have a close eye on on the participants here.

Yeah, I think that's and from memory the the molecule doesn't cross the bloodb brain barrier so that you've got um no central effects and that's going to mean that there's going to be less

interaction with the natural functioning of prolactin um and its regulation. But

like any clinical study there is a whole stratified program going through the phase one, two and three where any side effects will be closely monitored.

There's nothing there's no red flags at this stage, but certainly it's the same with any new molecule that uh that there's a process to go through and uh and there's no guarantees until you've

finished the process.

>> Thank you so much.

>> This concludes the Q&A section of the call. I would now like to turn the call

call. I would now like to turn the call back to the ABSI team for closing remarks.

Yeah. Well, first off, I just want to thank everyone for for joining. I hope

that this was uh educational uh from both a scientific perspective as well as a commercial perspective and uh want to thank the wonderful uh koss that that

joined uh today and uh gave their their perspective uh for for joining uh and look forward to to sharing the clinical data along the way um both uh with the

SAD and then the upcoming u MAD PC 13 week.

Thank you for joining us. Now

disconnect.